Fas ligand breaks tolerance to self-antigens and induces tumor immunity mediated by antibodies

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Item Type:	Article
Title:	Fas ligand breaks tolerance to self-antigens and induces tumor immunity mediated by antibodies
Creators Name:	Simon, A.K., Gallimore, A., Jones, E., Sawitzki, B., Cerundolo, V. and Screaton, G.R.
Abstract:	The role of Fas ligand (FasL) in programmed cell death via interaction with its receptor Fas is well characterized. It has been proposed that expression of FasL can confer immune privilege to some organs, allowing them to kill infiltrating lymphocytes and inflammatory cells. However, a number of studies have shown that when tumors or transplants express FasL, rejection often occurs as a consequence of proinflammatory functions of FasL. Here we demonstrate that FasL elicits tumor immunity in a murine melanoma model with weak immunogenicity and low expression of major histocompatibility complex (MHC) class I. We show that protected mice recognize melanocyte differentiation self-antigens. Importantly, tumor immunity is mediated by antibodies, as it can be transferred by serum from protected mice.
Keywords:	Neoplasm Antibodies, Autoantigens, Bone Marrow, Cell Differentiation, Cell Division, Immunologic Cytotoxicity, Dendritic Cells, Disease-Free Survival, Fas Ligand Protein, Flow Cytometry, Green Fluorescent Proteins, Immune Tolerance, Immunoglobulins, Lipopolysaccharides, Luminescent Proteins, Tumor-Infiltrating Lymphocytes, Melanocytes, Experimental Melanoma, Membrane Glycoproteins, Inbred C57BL Mice, T-Lymphocytes, Transfection, Cultured Tumor Cells, Animals, Mice
Source:	Cancer Cell
ISSN:	1535-6108
Publisher:	Cell Press / Elsevier
Volume:	2
Number:	4
Page Range:	315-22
Date:	October 2002
Official Publication:	https://doi.org/10.1016/s1535-6108(02)00151-4
PubMed:	View item in PubMed

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